Traumatic brain injury (TBI) may be caused by blunt injury (motor vehicle accident (MVA), falling or otherwise being struck in the head), penetrating injury (high velocity-bullet wound), or blast injury. Immediate neuronal, axonal and vascular destruction results from the impact of a blunt, bullet or blast injury. The amount of immediate tissue damage is highly variable depending upon the energy transfer at the point of impact and the medical status of the victim. In the civilian population, at least 200,000-300,000 significant blunt TBI events occur per year. Most of these are MVA, induced falls (particularly in the young and sports injuries), but bullet injuries may well add at least 25,000 more. Blast injury is the single largest killer of the “War on Terror”. Casualties are approximately 4,000 dead and perhaps 300,000 have had one or more blast injury TBI events. In blast injury the military medical research community is just beginning to study the mechanisms and predictability of the injury. The effects of multiple sub-lethal blast injuries to the brain and or spinal cord are not known. It is known that after TBI and spinal cord injury there is an ongoing series of events that leads to tissue damage over the next 7-10 days. The initial injury sets up cellular events of calcium flux, ion leakage, cellular apoptosis, vascular insufficiency, neutrophil activation, clot formation, edema etc. All of these mechanisms further feed back into the neuronal apoptosis and cell death mechanisms perpetuating the cycle.